Mechanosensing pathways in the progression of pulmonary fibrosis

Abstract

Fibrotic diseases are characterized by the excess production of extracellular matrix components that leads to changes in tissue mechanics and function. Mechanosensing altered during the onset of pulmonary fibrosis is hypothesized to form a positive-feedback loop that contributes to the progression of the disease. However, the exact mechanism(s) leading to fibrotic tissue remodeling as opposed to homeostatic tissue remodeling remains unknown. The development of innovative laboratory models of pulmonary fibrosis has facilitated mechanistic studies of pathogenic mechanosensing and identified new anti-fibrotic candidates. This brief review will cover recent (<5 years) publications that explore mechanotransduction pathways contributing to the development of pulmonary fibrosis and innovative laboratory models that can advance the field.